β-Adrenergic receptors (βAR) belong to the superfamily of G-protein coupled receptors (GPCRs). βAR stimulation by the sympathetic nervous system or circulating catecholamines is involved in peripheral blood circulation, metabolic regulation, muscle contraction, and central neural activities. In the heart, acute βAR stimulation serves as the most powerful means to regulate cardiac output in response to a fight-or-flight situation.

There are three βAR subtypes, β₁AR, β₂AR and β₃AR, in cardiac myocytes¹. The receptors consist of seven membrane-spanning domains, three intra- and three extracellular loops, an extracellular N-terminal domain, and an intracellular C-terminal tail².

β₁AR is the predominant receptor subtype expressed in human cardiomyocytes. β₁AR is also expressed in the kidney³. It has been implicated in adipogenesis and memory formation⁴.

β₁AR has been widely connected with heart disease. Both the downregulation and overstimulation of β₁AR have been connected to myocyte apoptosis. In addition, chronic heart failure is characterized by abnormalities in β₁AR signal transduction. It was demonstrated that heart failure is also inducible in animal models by overexpression of components of the β₁AR signal transduction cascade. Transgenic mice overexpressing β₁AR develop, with aging, heart failure similar to that observed in dilated cardiomyopathy in humans⁵.